1. Field of the Invention
This invention is directed to methods of treating diseased, non-aneurysmal arteries with vascular reconstruction.
Specifically, the methods of this invention can be used to remodel blood flow pathways, redirect blood flow patterns, and to seal off undesired blood flow pathways. The methods of this invention can be used to treat a variety of diseased arteries in need of vascular reconstruction. For instance, the invention can be used to treat fistulas and other vascular abnormalities. In addition, the invention can be used to treat vascular walls which have suffered traumatic tears, punctures or dissections. The methods of this invention can also be used to treat or prevent stenosis in arteries which have undergone angioplasty. The present invention can even be used as an alternative to angioplasty.
References
The following publications are cited in this application as superscript numbers:                1 Dunn, et al., U.S. Pat. No. 4,938,763 for “Biodegradable In-Situ Forming Implants and Methods of Producing Same”, issued Jul. 3, 1990        2 Kinugasa, et al., “Direct Thrombois of Aneurysms with Cellulose Acetate Polymer”, J. Neurosurg., 77:501–507 (1992)        3 “CANCER, Principles & Practice of Oncology”, 4th Ed., Volume 1, “Cancer Treatment”, pp. 545–548 (1993)        4 Greff, et al., U.S. Pat. No. 5,667,767, for “Novel Compositions for Use in Embolizing Blood Vessels”, issued Sep. 16, 1997        5 Greff, et al., U.S. Pat. No. 5,580,568 for “Cellulose Diacetate Compositions for Use in Embolizing Blood Vessels”, issued Dec. 3, 1996        6 Kinugasa, et al., “Early Treatment of Subarachnoid Hemorrhage After Preventing Rerupture of an Aneurysm”, J. Neurosurg., 83:34–41 (1995)        7 Kinugasa, et al., “Prophylactic Thrombosis to Prevent New Bleeding and to Delay Aneurysm Surgery”, Neurosurg., 36:661 (1995)        8 Taki, et al., “Selection and Combination of Various Endovascular Techniques in the Treatment of Giant Aneurysms”, J. Neurosurg., 77:37–24 (1992)        9 Evans, et al., U.S. patent application Ser. No. 08/802,252 for “Novel Compositions for Use in Embolizing Blood Vessels”, filed Feb. 19, 1997        10 Castaneda-Zuniga, et al., Interventional Radiology, in Vascular Embolotherapy, Part 1, 1:9–32, Williams & Wilkins, Publishers (1992)        11 Rabinowitz, et al., U.S. Pat. No. 3,527,224 for “Method of Surgically Bonding Tissue Together”, issued Sep. 8, 1970        12 Hawkins, et al., U.S. Pat. No. 3,591,676 for “Surgical Adhesive Compositions”, issued Jul. 6, 1971        13 Laird, et al., “Inhibition of Neointimal Proliferation With Low-Dose Irradiation From a β-Particle Emiting Stent,” Circulation 93(3):529–536 (1996)        14 Greff, et al., U.S. patent application Ser. No. 08/962,819, Radioactive Embolizing Compositions, filed Nov. 3, 1997.        15 Hemphill, III, et al., “Endovascular Therapy of Traumatic Injuries of the Intracranial Cerebral Arteries”, Endovascular Therapy and Neurocritical Care 15 (4): 811–829 (October, 1999).        16 Gomez, et al., “Endovascular Theraphy of Traumatic Injuries of the Extracranial Cerebral Arteries”, Endovascular Therapy and Neurocritical Care 15 (4): 789–809 (October, 1999).        
All of the above publications are herein incorporated by reference in their entirety to the same extent as if each individual reference was specifically and individually indicated to be incorporated herein by reference in its entirety.
2. State of the Art
Vascular reconstruction involves the non-endogenous reformation of arterial vessels in order to prophylactically or therapeutically treat one or more arterial disease conditions in a mammal. Examples of diseased arterial conditions include, for instance, high flow fistulas, dissections, and restenosis of the arterial endothelial wall after balloon angioplasty to treat atherosclerosis.
1. Dissections
Dissections occur when injury to one or more arterial layers allows blood to force its way along a dissection plane.15 In the most common type of dissection, an injury or defect occurs in the intima layer of the blood vessel, causing blood to pool between the intima and media layers. The blood that collects below the intima layer may push it towards the interior of the lumen. The dissection may cause a flap of the intima to extend out into the lumen. This flap can collect embolic material or possibly even occlude the lumen.
In other instances, the dissection can occur between the media and adventicia layers. Here, the pooling of blood in the dissection can lead to either a subarachnoid hemorrhage or the formation of a pseudoaneurysm.15 
2. Fistulas
Fistulas involve abnormal connections between arterial and venous circulations which can cause inadequate perfusion of affected tissue.15 Fistulas can be “direct”, meaning that there is a complete disruption of the wall of an artery, with connection directly into the venous circulation. Alternatively, fisulas can be “indirect”, meaning that arteriovenous connections are located within the dura.
3. Atherosclerosis
In the case of atherosclerosis, this arterial disease involves thickening and hardening of the wall portions of the larger arteries of mammals. It is a life-threatening affliction that is largely responsible for coronary artery disease, aortic aneurysm and arterial disease of the lower extremities. Atherosclerosis also plays a major role in cerebral vascular disease. It is responsible for more deaths in the United States than any other disease.
Angioplasty has heretofore been a widely used method for treating atherosclerosis. Percutaneous transluminal coronary angioplasty (hereinafter “PTCA”) procedures involve inserting a deflated balloon catheter through the skin and into the vessel or artery containing the stenosis. The catheter is then passed through the lumen of the vessel until it reaches the stenoic region, which is characterized by a build up of fatty streaks, fibrous plaques and complicated lesions on the vessel wall, which result in a narrowing of the vessel and blood flow restriction. In order to overcome the harmful narrowing of the artery caused by the atherosclerotic condition, the balloon is inflated, thus flattening the plaque against the arterial wall and otherwise expanding the arterial lumen.
Although PTCA has produced excellent results and low complication rates, there has, however, been difficulties associated with the use of this technique. In particular, during the expansion of the balloon against the arterial wall, the arterial wall is frequently damaged and injured. While this damage itself is not believed to be particularly harmful to the health or the life of the patient, the healing response triggered by this damage can cause a reoccurrence of the atherosclerotic condition. In particular, it has been observed that the smooth muscle cells associated with the stenotic region of the artery initiate cell division in response to direct or inflammatory injury of the artery.
Restenosis is the closure of a peripheral or coronary artery following trauma to the artery caused by efforts to open an occluded portion of the artery, such as, for example, by dilation, ablation, atherectomy or laser treatment of the artery. For these angioplasty procedures, restenosis occurs at a rate of about 20–50% depending on the vessel location, lesion length and a number of other variables. Restenosis is believed to be a natural healing reaction to the injury of the arterial wall that is caused by angioplasty procedures. The healing reaction begins with the clotting of blood at the site of the injury. The final result of the complex steps of the healing process is intimal hyperplasia, the migration and proliferation of medial smooth muscle cells, until the artery is again stenotic or occluded.
In an attempt to prevent restenosis, metallic intravascular stents have been permanently implanted in coronary or peripheral vessels. The stent is typically inserted by catheter into a vascular lumen and expanded into contact with the diseased portion of the arterial wall, thereby providing internal support for the lumen. However, it has been found that restenosis can still occur with such stents in place. Without being limited to any theory, it is believed that the in situ placed stent does not isolate the arterial wall from the oxygen/nutrients of the blood necessary for smooth muscle cell proliferation which is the seminal event in restenosis.